Feb 9, 2013

Original full version “Radioactive Caesium and Heart”https://docs.google.com/file/d/0B3fFCVXEJlbvQkluX2tocjVZd2c/edit
Thus, it is possible to make a conclusion about harmful influences
of this radionuclide on the cardiovascular system after analyzing the
following data: results of ECG examination of the children of various
ages with varying degrees of incorporation of radioactive cesium in the
body; microscopic studies of organs of individuals in the territories
affected by the Chernobyl accident; and lastly laboratory experiments
with animals. This effect is manifested not only due to its direct
impact on cellular structures but also its indirect influences through a
series of systems, in particular the nervous and endocrine systems.
A direct effect of radioactive cesium on the heart is due to its
selective accumulation in the myocardial cells compared to other organs
and tissues (Fig. 9 &10). Perhaps it is due to the intensive
functioning of the Na+/K+
pump: since Cs-137 is similar to potassium, it is absorbed by
cardiomyocytes fairly easily. This process involves the structures of
cellular membranes, and this radionuclide interacts with them easily.15
This is accompanied by suppression of a very essential enzyme such as
creatine phosphokinase, which is involved in the cellular energetic
metabolism: accumulation, transport, and utilization of high energy
phosphates. Creatine phosphokinase (CPK) catalyzes the reversible
phosphorylation reaction which involves transfer of a phosphate group
from adenosine triphosphate (ATP) to creatine and from phosphocreatine
to adenosine diphosphate (ADP). 1Figure 9. Accumulation of Cs-137 in organs and bodies of experimental animals1-heart, 2-liver, 3-spleen, 4-kidneys, 5-whole bodyFigure 10. Accumulation of Cs-137 in the internal organs of albino rats with a daily intake of 180 Bq 1-whole body, 2-liver, 3-kidneys, 4-myocardium, 5-spleen, 6-skeletal muscles, 7-testicles, 8-lungs
Creatine phosphokinase is localized in different subcellular
structures: cytoplasm, mitochondria, microsomes, nuclei, sarcoplasmic
reticulum and myofibrils. According to the existing concept,
mitochondrial creatine phosphokinase catalyzes the formation of
phosphocreatine from ATP, which is produced within the mitochondrial
matrix as a result of oxidative phosphorylation. The resulting
phosphocreatine moves into the cytoplasm according to the concentration
gradient or by rapid diffusion to specific isoenzymes of creatine
phosphokinase and in particular to be:

· related to the structures responsible for muscle contraction; the M-line of myofibrils.· associated with the sarcoplasmic reticulum Ca2+ adenosine triphosphatase.

· related to the sarcoplasm and the Na+/K+ adenosine triphosphatase.· associated with postsynaptic membrane, rich in acetylcholine receptors and ATPases.
Mitochondrial creatine phosphokinase holds together the outer and
inner surfaces of the mitochondrial membrane, creating its structure.1
Localization of creatine phosphokinase in the area of M-line
creates conditions that allow continuous renewal of ATP to ensure proper
contractile function of myofibrils (Fig. 11). The resulting creatine
returns to mitochondria in order to again become a substrate for
phosphorylation. Figure 11. Intercalated disks of cardiac muscles (scheme).1-basement
membrane of cardiomyocyte, 2-sarcolemma of cardiomyocyte,
3-mitochondrion, 4-myofibrils, 5-sarcoplasma, 6-cytoplasmic network,
7-thin filament (actin), 8-thick filament (myosin), 9-intercalated disk,
10-light disk (I-band), 11-dark disk (A-band), 12-Z disk, 13-M-disk,
14-desmosome (macular adherans), 15 nexus (gap junction), 16-fascia
adherens (by Bargmann & Schulce; modified).
Thus a decrease in the enzyme activity indicates serious structural
and metabolic defects in the energetic complex of cardiomyocytes. This
is observed as changes in the mitochondrial system in the form of an
increase in the number and size of mitochondria and the increase in the
number of lamellar cristae and their subsequent destruction. It is also
observed as aggregation of mitochondria and changes in the number of
intermitochondrial contacts (Fig.12).

Figure
12. Aggregation, increase in the number, and increase in the size of
mitochondria of cardiomyocytes of rats with incorporation of radioactive
cesium in the body at 45 Bq/kg. Magnification X30,000.
Inhibition of the energy complex could be related to a direct
influence of radioactive cesium on the membrane structure as well as an
influence of several metabolites, particularly thyroid hormones,
considering that these hormones have toxic effects on the mitochondrial
system. 13 In
this regard, activities of creatine phosphokinase are inhibited in
Graves’ disease or in experimentally induced hyperhyroidism. 1 It
is possible that under the influence of radioactive cesium an increased
amount of free thyroxin damages myocardial cells by affecting these
enzymes. This hypothesis is proven by the increase in the frequency of
ECG changes that parallels the free thyroxine level in blood of children
with radioactive cesium incorporation of higher than 37 Bq/kg (Fig.
13). Thus it is possible to assume the role of thyroxin in occurrence
of arrhythmias.

Figure
13. Dependence of serum thyroxine (T4) level in children on the amount
of incorporated Cs-137 (P <0.001 between Groups 1 and 3). In men, activity of creatine phosphokinase is greater than in women. 1
It cannot be ruled out that the vulnerability of this enzyme in
myocardial cells under the influence of radioactive cesium is the
leading cause of sudden deaths in men.8,29,41
It should be noted that a decrease in the activity of alkaline
phosphatase in the myocardial structures is indicative of the
development of degenerative processes specific for exposure to ionizing
radiation. 36
The nature of structural changes, in the myocardial cells of
laboratory animals with the incorporation of radioactive cesium and
individuals living in areas contaminated with radioactive cesium,
indicates impairment of permeability of sarcoplasmic reticulum membrane
for Ca2+.
This may be due to the direct effect of this radionuclide on the cell
membrane as well as the radioactive rays emitted as it decays. The
resulting peroxidation of fatty acid chains of phospholipids leads to
changes in the cell membrane’s structure and permeability to different
ions, including Ca2+
. At the same time, it naturally changes the activity of
membrane-bound enzymes. Excess production of free hydroxy radicals and
amplification of lipid peroxidation contribute to the destruction of
cell membranes. The Ca2+
transport system of the myocardial sarcoplasmic reticulum is actively
involved in the process of contraction-relaxation of myofibrils by way
of releasing and accumulation of Ca2+. If the system is damaged due to various agents, including radioactive cesium, the level of free Ca2+ in cardiomyocytes increases and the relaxation of myofibrils is disrupted.
Changes in the contractile apparatus are reflected in changes
observed in the double ray refraction of myofibrils: appearance of
segmental and subsegmental contractures, intracellular myocytolysis,
primary cluster disintegration of myofibrils, cytolysis, and eventually
coagulative or colliquative necrosis. 32
Contractive alterations of segmental and subsegmental types are
defined in the polarized light by enhancement of the anisotropy of the
A-band of myofibrils. They look like a radiant cross strip with cross
sections of striated myofibrils between them. When examined under the
light microscope, they are visible due to the greater density and
eosinophilia. Ten days’ worth of radioactive cesium incorporation by
rats of Vistar line (cesium concentration was 60-100 Bq/kg) also led to
these alterations (Fig. 14).

In
the primary cluster disintegration of myofibrils, the isotropic spaces
are found between anisotropic clusters (Fig 15). This, unlike
contractures, is severe and irreversible damages to cardiomyocytes
indicating their death. It should be noted that primary cluster
disintegration is often found in acute cardiac insufficiency. 30,31Figure
15. Histological section of myocardium of a woman who died in
childbirth. Radioactive cesium concentration in heart at 105 Bq/kg.
Primary cluster disintegration of myofibrils. Loosening of muscle
fibers. Intermuscular edema. Stained with hematoxylin and eosin.
Magnification X250.Cytolysis or in vivo autolysis of myocardiocytes is also an
irreversible condition. It tends to be diffuse under the influence of
radioactive cesium (Fig. 16,17).Figure
16. Histological section of animal myocardium after incorporation of
radioactive cesium (concentration in the body at 900 Bq/kg). Diffuse
myocytolysis. Pronounced intertissue edema. Stained with hematoxylin
and eosin. Magnification X125.Figure
17. Histological section of myocardium of a 43-year-old Dobrush
resident who died suddenly. Raioactive cesium concentration 45 Bq/kg.
Diffuse myocytolysis. Intermuscular edema. Fragmentation of muscle
fibers. Stained with hematoxylin and eosin. Magnification x125.
The above changes are observed not only under the exposure to
radioactive cesium but also when there are metabolic damages due to
intoxication, hypoxia, or functional overload 14,24,40 and under the influence of extreme environmental factors contributing to the development of stress reactions. 27,28,31 It is observed that these reactions occur when the Ca2+ concentration in cardiomyocytes is increased. 28
The leading role in the mechanism of injury is played by the
effects of catecholamines (noradrenaline, adrenaline) on the
beta-adrenergic receptors of the myocardium. This does not have any
connection with ischemic damage to the heart. 28
The total scheme of the effects on heart is influenced by a wide
variety of factors through stress reactions. High concentrations of
catecholamines increase the number and timing of opening of the
voltage-dependent and receptor-dependent calcium channels, resulting in
the accumulation of Ca2+ in
cardiomyocytes. In addition, cells of conducting system are damaged
earlier and to a greater degree, since they have low resting potential
and the input ion current, which is responsible for the action
potential, is primarily calcium.10 Moreover, this system has predominantly adrenergic innervation. 28 As a result of the process, cells end up with a high concentration of Ca2+. When these Ca2+
are inappropriately released from the cell, arrhythmias, or rhythm
disturbances can occur. We emphasize that it is directly related to the
function of the cationic pumps. A significant role in the energy
supply for the pump is played by the creatine phosphokinase and
glycolytic systems. 28
In order to cause relaxation of myocardium and break bridges between
thin actin and thick myosin myofibrils, it is necessary to coordinate
both of these systems. This includes sarcoplasmic reticulum ATPase,
which transports Ca2+
back into the cistern of sarcoplasmic reticulum. It should be noted
that this is an energy-requiring process, comprising nearly 15% of all
energetic consumption of the cardiac muscles. 25Considering
the duration of influence of radioactive cesium on people living in the
contaminated territories and the suppression of noradrenaline
production in the cells of cerebral hemispheres, 23
it is not hard to imagine the leading role of catecholamines in causing
contractures of muscle fibers. It could just happen in cases of strong
stress reactions. In reality, accumulation of Ca2+
in the cells under the influence of radioactive cesium can occur due to
the energy deficit caused by damage to the energy supply system within
the cell membranes, including mitochondria and structures of
sarcoplasmic reticulum. That is why the cells cannot release Ca2+
in a timely manner. Calcium ions enter the cells very intensively due
to the destruction of membrane phospholipids by free radical hydroxyl
groups. In this situation it does not take much effort to cause
significant myocardial damage. Death of cardiomyocytes can occur due to
prolonged energy deficits, caused by physical exertion, acute
infectious processes and alcohol intoxication.
Cardiac activity could be stopped by increasing the concentration
of radioactive cesium in the body. In particular, a rapid
administration of a large amount of the Cs-137 radionuclide, reaching
the concentration of 1,000 Bq/kg within 5 days, caused cardiac arrest in
rats. In this case the radioactive agent itself became the direct
cause of death. To a lesser degree, the source of recontractions of
myofibrils of cardiomyocytes in the presence of radioactive cesium
accumulation could be an emotional stress, resulting in the release of
catecholamines. This is due to the fact that in long-term cesium
toxicity, there is a progressive suppression of function of the
sympathetic nervous system, reducing the adaptive reserve of the body.17
At the same time it is impossible to exclude the role of
catecholamines in cardiac damage under the influence of radioactive
cesium.
This has been confirmed by the results of clinical and laboratory
testing of children with chronic gastrointestinal pathology. There was a
directly proportional relationship between the frequency of
hypersympatheticotonic variant of the autonomic nervous system
reactivity and the amount of radioactive cesium in the body. Based on
the above data, it is necessary to conclude that the energy deficit in
the calcium transport system, appearing during the radioactive cesium
incorporation, leads to disruption of cardiac rhythm, disorders of
contractile apparatus of cardiomyocytes, and eventually cardiac arrest.
Injuries to the cardiovascular system could not be examined
separately from other organs and systems, particularly the kidneys. As
the main organ of excretion of radioactive cesium from the body,16 kidneys
are significantly affected even at a small Cs-137 concentration.
Kidneys also undergo similar damaging effects as the cardiovascular
system, first and foremost in the glomerular apparatus. 6,7
In the muscle fibers within the arterioles, there are changes
identical to those observed in the myocardium. Contractures of
myofibrils lead to a prolonged spasm of the arterioles, stopping the
circulation in the structures of the nephron. Deaths of cellular
elements form a specific structural change in the glomeruli, a
phenomenon called melting icicles. Dystrophic and necrobiotic changes
gradually appear, accompanied by wrinkling and fragmentation of the
glomeruli (Fig. 18 &19). Figure
18. Histological section of albino rat kidney with a radioactive cesium
concentration in the whole body at 900 Bq/kg. Necrosis and
fragmentation of glomeruli with cavity formation. Necrosis and hyaline
droplet dystrophy of tubular epithelium. Stained with hematoxylin and
eosin. Manification x250.Figure
19. Histological section of kidney of a 71-year-old female patient in
Gomel. She died of adhesions of abdominal cavity and right lung acute
lobar pneumonia with consolidation and fibrino-purulent component,
complicated by bilateral pulmonary edema. Radioactive cesium
concentration in kidneys was 300 Bq/kg. Fluid accumulation in
glomerular cavities. Hyaline droplets and hydropic dystrophy of tubular
epithelium. Interstitial tissue edema. Stained with hematoxylin and
eosin. Magnification x125.

Cavity
formation without any marked cellular reaction is typical as the
influence of radioactive cesium on kidney’s tissues. With the ability
to cause hyper-contractions (excess contractions) of muscle fibers in
arterioles, this radionuclide damages the processes of vascular
microcirculation in kidneys. It should be noted that there is an
absence of necessary inflammatory reactions of the body in response to
the damages in kidneys and other organs. In our opinion, this is due to
the suppression of synthesis of biologically active substances, such as
inflammatory mediators, in specialized cells.
Damaged glomeruli cease functioning. Histologic characteristics of
kidneys under the influence of radioactive cesium are the same as those
of thrombotic microangiopathy. 2
This is no coincidence. In both cases, the microcirculatory
channeling system of nephron is blocked at the level of arterioles,
leading to necrobiotic processes.
Development of renal insufficiency is the reason for accumulation
of metabolic waste products in the body. They have toxic effects, along
with the toxic effects of radioactive cesium itself, on the vital
organs and systems. Also characteristic are the inflammatory processes
of serous membranes, particularly of pericardium (Fig. 20) and pleura
(Fig. 21).Figure
20. Histological section of animal myocardium with Cs-137 incorporation
at 900 Bq/Kg in the body. Infiltration of epicardium and pericardium
with neutrophils and lymphocytes. Pronounced myocytolysis. Stained
with hematoxylin and eosin. Magnification x125.

Figure
21. Histological section of animal lung with Cs-137 incorporation at
900 Bq/kg in the body. Plethora from rupture of blood vessels in the
alveolar lumen. Infiltration of visceral pleura with neutrophilic
leukocytes, lymphocytes and histiocytes. Stained with hematoxylin and
eosin. Magnification x125.
Injuries to the vascular system of kidneys may be one of the main
reasons for the increase in blood pressure, especially diastolic
pressure, in children. However, considering the hidden, latent course
of this pathological process, it could only manifest later, after
ordinary medical treatments proved insufficient. Therefore, regular
assessment of kidney and cardiac function must be done in children
living in areas contaminated with radioactive cesium, using modern
laboratory and technological diagnostic methods.
Liver is also negatively affected by the influence of radioactive
cesium. Individuals who lived in the Gomel region had significant
levels of radioactive cesium in their liver. 6
In most of those cases, histologic examinations revealed marked
dystrophic and necrobiotic changes in the hepatocytes (Fig. 22).Figure
22. Histological section of liver from a 40-year-old Gomel resident
who died of sudden death. Radioactive cesium concentration in the liver
was 142 Bq/kg. Fat and protein degeneration with necrosis of
hepatocytes. Stained with hematoxylin and eosin. Magnification x125.
Similar changes were observed in the experimental animals under the
influence of radioactive cesium. Immediately there was a disruption of
the hepatocyte function, particularly synthetic and detoxifying
functions.
Impairment to the synthetic function of hepatocytes is manifested
as a progressive decrease in the synthesis of L1-globulin and
L2-globulin with an increasing concentration of radioactive cesium in
the body. This will undoubtedly affect the state of metabolism in other
organs, including the heart.
Oxidation of steroid hormones, especially the adrenal cortical
hormones, takes place in the liver. Also destruction of catecholamines,
the hormones of adrenal medulla, noradrenaline and adrenalin, takes
place by way of methylation reaction. A huge role of liver is
detoxification of ammonia, by utilizing it in the synthesis of urea.
Inefficiency in both synthetic and detoxifying functions of liver leads
to the appearance of metabolic dysfunction, which leads to an adverse
effect on the state of myocardium.
Thus, metabolic dysfunction, occurring in the body incorporating
radioactive cesium, may contribute to disturbances in the structure and
function of cardiomyocytes.

Conclusion

While working on this book, I kept thinking about the need to
inform every civilized individual of the dangers of radioactive
substances when incorporated into the body. Unfortunately, the attitude
of the present society to this issue is, at best, indifference. We pay
a very high price for this in the form of human lives. Intelligent
ignorance leads to a tragedy. To a great extent the blame rests on
medical scientists. Not only did they not try to inform population
using previously obtained data, but they did not study adverse changes
in the body due to incorporation of radionuclides.
I am aware that this little book cannot make up for the lack of
information on the existing problem. Nevertheless, I hope it will
raise some interest, leading to discussion of the problem. This will
undoubtedly be helpful. Based on the information presented, some conclusions can be drawn.
Whether we like it or not, radionuclides, especially radioactive
cesium, are present in our environment. Without any protective
measures, they enter a human body mainly through food and water,
becoming incorporated in organs and tissues. The greatest danger to
human life represents the incorporation of radioactive cesium in the
cardiac muscles of growing bodies.
When myocardial cells are penetrated by the radionuclide Cs-137,
structural and metabolic changes follow, leading to the energy deficits
and disruption of their main functions, and in some cases death. A
series of changes occur, indicating direct damage of the cardiac muscles
as well as damage to many organs and systems regulating its activity.
Cardiomyocytes are damaged not only directly due to radioactive cesium
but also due to natural metabolites when there is disruption in their
production, transport, binding, excretion, and degradation (Fig. 23).

Figure 23. Diagram for the influence of radioactive cesium on cardiomyocytes(CPK=creatine phosphokinase, ATP=adenosine triphosphate)
Degree of severity of pathological changes is directly dependent on
the amount of radioactive cesium in the body and cardiac muscles.
Long-term incorporation of the radionuclide in the body greater than 30
Bq/kg is highly undesirable, possibly leading to serious consequences.
In most cases the effect of existing concentration of radioactive
cesium in the body (10-20 Bq/kg) does not lead to death. However, the
influence of radioactive cesium on the energy apparatus of
cardiomyocytes significantly reduces their adaptive capacity. It might
become impossible to function in a variety of stressful and ordinary
situations, such as physical and mental stress, hypoxia, extreme
temperature fluctuations, drinking alcohol, infections, and allergic
diseases.
It should be recognized that radioactive cesium is a potent
damaging agent and it should be treated as a delayed poison to cell
actions.
Undermining the energetic mechanism for cardiomyocytes, it causes
cardiomyopathy, characterized by cardiac rhythm disturbances,
abnormalities in myocardial contractility, and spasms of peripheral
blood vessels. It should be noted that the effect of incorporated
radioactive cesium on humans and animals suggests its involvement in
energetic and metabolic processes, primarily as a chemical element
rather than a source of radiation. Nevertheless, the latter
involvement, as a source of radiation, cannot be excluded completely.
This is especially pronounced with prolonged exposure to small amounts
of this radionuclide. The main reason for pathological changes of the
kidney due to the influence of radioactive cesium is arteriole spasm,
which causes necrosis of the glomerular loops and destruction of the
nephron structures. The vasoconstrictive effect of cesium was noted by
S.S. Botkin in 1888. 11
Therefore, radioactive cesium is one of the major etiologic factors
in high blood pressure in children living in radioactively contaminated
areas. This has been confirmed by numerous observations. 20
As the basis of prophylaxis of cardiovascular diseases in
population living in the areas affected by the Chernobyl accident,
relevant issues include the reduction of the amount of radionuclides,
above all radioactive cesium, by reduction of its content in food as
well as its elimination from the body with adsorbing agents. These
measures will play an important role in improving the metabolism of
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